Electrophysiology in the time of coronavirus: coping with the great wave.

Jia Li; Patrizio Mazzone; Lisa Leung; Weiqian Lin; Giuseppe D'Angelo; Jun Ma; Jin Li; Zaki Akhtar; Yuechun Li; Paolo E Della Bella; Jiafeng Lin; Mark M Gallagher

Severe acute respiratory syndrome coronarvirus-2 (SARS-CoV-2), the agent responsible for COVID-19 has an affinity for angiotensin converting enzyme 2 (ACE2) receptors. 11 This is central to the pathophysiology of the condition, leading to pneumonia and in critical stages, associated fulminant acute respiratory distress syndrome (ARDS) and multi-organ failure. 12 The primary affected organ is the lung but cardiovascular injury is also common. There is enhanced expression of ACE-2 in those with cardiovascular conditions, possibly accounting for the apparent greater severity of COVID-19 related illness in these patients. In one study, a majority (58%) of those with severe infection had a background of hypetension, and non-specifically 44% had a history of 'arrhythmia'. 13 Binding of the virus to ACE2 receptors in the lung and the heart initiates the acute inflammatory response. Pneumonia results, but also evidence of myocarditis; those with a rise in high-sensitivity Troponin I are more likely to require admission to intensive care. 14 There is a strong association between a history of hypertension and mortality from COVID-19. Systolic blood pressure was significantly higher in those with COVID-19 treated in intensive care units compared to those not requiring this level of care (144 versus 122, P<0.001). 14 This may relate to up-regulation of ACE2 receptors in those receiving ACE inhibiting drugs. All rights reserved. No reuse allowed without permission. author/funder, who has granted medRxiv a license to display the preprint in perpetuity.